Search results for "inflammation."

showing 10 items of 2627 documents

Transforming growth factor β (CiTGF-β) gene expression is induced in the inflammatory reaction of Ciona intestinalis.

2016

Transforming growth factor (TGF-β) is a well-known component of a regulatory cytokines superfamily that has pleiotropic functions in a broad range of cell types and is involved, in vertebrates, in numerous physiological and pathological processes. In the current study, we report on Ciona intestinalis molecular characterisation and expression of a transforming growth factor β homologue (CiTGF-β). The gene organisation, phylogenetic tree and modelling supported the close relationship with the mammalian TGF suggesting that the C. intestinalis TGF-β gene shares a common ancestor in the chordate lineages. Functionally, real-time PCR analysis showed that CiTGF-β was transcriptionally upregulated …

0301 basic medicineLipopolysaccharidesCell typeHemocytesTGFbeta Ciona intestinalisCellular differentiationImmunologyMolecular Sequence DataSettore BIO/05 - ZoologiaBiology03 medical and health sciences0302 clinical medicineImmune systemTranscription (biology)Transforming Growth Factor betaGene expressionAnimalsCiona intestinalisAmino Acid SequenceCloning MolecularGenePhylogenyInflammationMammalsbiology.organism_classificationImmunity InnateCell biologyCiona intestinalisUp-Regulation030104 developmental biologyImmunologyPharynx030217 neurology & neurosurgeryDevelopmental BiologyTransforming growth factorDevelopmental and comparative immunology
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Molecular characterisation, evolution and expression analysis of g-type lysozymes in Ciona intestinalis

2017

Lysozyme is an important defense molecule of the innate immune system. Known for its bactericidal properties, lysozyme catalyzes the hydrolysis of b-(1,4)-glycosidic bonds between the N-acetyl glucosamine and N-acetyl muramic acid in the peptidoglycan layer of bacterial cell walls. In this study, the complete coding sequence of four g-type lysozymes were identified in Ciona intestinalis. Phylogenetic analysis and modelling supported the hypothesis of a close relationship with the vertebrate g-type lysozymes suggesting that the C. intestinalis g-type lysozyme genes (CiLys-g1, Cilys-g2, CiLys-g3, CiLys-g4) share a common ancestor in the chordate lineage. Protein motif searches indicated that …

0301 basic medicineLipopolysaccharidesImmunologySettore BIO/05 - ZoologiaChordateBacterial cell structureMicrobiologyEvolution Molecular03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBacteriolysisGeeseAnimalsCiona intestinalisCloning MolecularStructural motifGeneCells CulturedPhylogenyInnate immune systembiologyBacterial Infectionsbiology.organism_classificationBiological EvolutionImmunity InnateCiona intestinalisAscidian Lysozymes g-type Inflammation LPS Ciona intestinalis030104 developmental biologyBiochemistrychemistry030220 oncology & carcinogenesisPharynxMuramidasePeptidoglycanLysozymeTranscriptomeDevelopmental Biology
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Investigating fibrosis and inflammation in an ex vivo NASH murine model.

2020

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, characterized by excess fat accumulation (steatosis). Nonalcoholic steatohepatitis (NASH) develops in 15–20% of NAFLD patients and frequently progresses to liver fibrosis and cirrhosis. We aimed to develop an ex vivo model of inflammation and fibrosis in steatotic murine precision-cut liver slices (PCLS). NASH was induced in C57Bl/6 mice on an amylin and choline-deficient l-amino acid-defined (CDAA) diet. PCLS were prepared from steatohepatitic (sPCLS) and control (cPCLS) livers and cultured for 48 h with LPS, TGFβ1, or elafibranor. Additionally, C57Bl/6 mice were placed on CDAA diet for 12 wk to receive elafibranor…

0301 basic medicineLipopolysaccharidesLiver CirrhosisMalePhysiologyHEPATOCYTESLiver diseaseMice0302 clinical medicineChalconesFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCells CulturedINSULIN-RESISTANCEGastroenterologyElafibranorTGF-BETALiver030211 gastroenterology & hepatologyCHOLINE-DEFICIENT DIETEXPRESSIONmedicine.medical_specialtyEARLY-ONSETIn Vitro TechniquesCollagen Type IProinflammatory cytokineTransforming Growth Factor beta103 medical and health sciencesIn vivoPhysiology (medical)Internal medicinemedicineAnimalsHEPATIC STEATOSISFATTY LIVER-DISEASEInflammationPRECISION-CUT LIVERHepatologybusiness.industrymedicine.diseaseLipid MetabolismDietMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyPROLIFERATOR-ACTIVATED RECEPTORSSteatosisPropionatesbusinessTranscriptomeEx vivoAmerican journal of physiology. Gastrointestinal and liver physiology
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Neonatal NET-inhibitory factor and related peptides inhibit neutrophil extracellular trap formation.

2016

Neutrophil granulocytes, also called polymorphonuclear leukocytes (PMNs), extrude molecular lattices of decondensed chromatin studded with histones, granule enzymes, and antimicrobial peptides that are referred to as neutrophil extracellular traps (NETs). NETs capture and contain bacteria, viruses, and other pathogens. Nevertheless, experimental evidence indicates that NETs also cause inflammatory vascular and tissue damage, suggesting that identifying pathways that inhibit NET formation may have therapeutic implications. Here, we determined that neonatal NET-inhibitory factor (nNIF) is an inhibitor of NET formation in umbilical cord blood. In human neonatal and adult neutrophils, nNIF inhi…

0301 basic medicineLipopolysaccharidesMaleExtracellular TrapsNeutrophilsAntimicrobial peptidesInflammationSystemic inflammationExtracellular TrapsHistones03 medical and health sciencesmedicineAnimalsHumansCells CulturedInflammationbiologyInfant NewbornGeneral MedicineNeutrophil extracellular trapsBlood ProteinsChromatin Assembly and DisassemblyFetal BloodMolecular biologyIn vitroCell biologyNeoplasm ProteinsMice Inbred C57BLHistone citrullination030104 developmental biologyHistonebiology.proteinmedicine.symptomProtein Processing Post-TranslationalResearch ArticleThe Journal of clinical investigation
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Glucagon-like peptide-1 is associated with poor clinical outcome, lipopolysaccharide translocation and inflammation in patients undergoing cardiac su…

2020

International audience; Introduction: Cardiac surgery with cardiopulmonary bypass (CPB) is associated with gut barrier dysfunction. Gut barrier dysfunction might be estimated non-invasively by lipopolysaccharide (LPS) plasma concentration. Glucagon-like peptide-1 (GLP-1) is a gut secreted hormone that is a potential marker of mucosal integrity. Our objective was to evaluate GLP-1 as a peri-operative marker of gut barrier dysfunction in patients undergoing cardiac surgery with CPB.Methods: GLP-1, intestinal fatty acid binding protein (I-FABP) and lipopolysaccharide were assayed: at induction, after CPB and 24 h after admission in the intensive care unit. The primary end-point was peri-operat…

0301 basic medicineLipopolysaccharidesMaleLipopolysaccharideBiochemistryGastroenterologylaw.inventionchemistry.chemical_compound0302 clinical medicinelawGlucagon-Like Peptide 1Gut barrierImmunology and AllergyProspective StudiesCardiopulmonary Bypassdigestive oral and skin physiologyHematologyCardiac surgeryMiddle AgedCardiopulmonary by passIntensive care unitGlucagon-like peptide-1Digestive translocation3. Good healthCardiac surgeryGlucagon like peptid 1030220 oncology & carcinogenesisFemalemedicine.symptommedicine.medical_specialtyImmunologyInflammationLipopolysaccharide03 medical and health sciencesInternal medicineIntensive caremedicineCardiopulmonary bypassHumansCardiac Surgical ProceduresMolecular BiologyAgedInflammationbusiness.industryEndotoxemia030104 developmental biologychemistrybusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBiomarkersHormoneCytokine
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Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses

2017

Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, b…

0301 basic medicineLipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharideFeverCell- och molekylärbiologiImmunologyHypothalamusAnorexiaEtanerceptInterleukin-1 type 1 receptor; Lipopolysaccharide; Fever; Anorexia; ACTH; Corticosterone; Endothelial cells; THF alpha; Interleukin-6; PGE(2)03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundEating0302 clinical medicineAdrenocorticotropic HormoneCorticosteroneInternal medicinemedicineJournal ArticleAnimalsInterleukin 6ReceptorIllness BehaviorInflammationMice KnockoutReceptors Interleukin-1 Type IbiologyEndocrine and Autonomic Systemsbusiness.industryInterleukinBrainEndothelial CellsAnorexia030104 developmental biologyEndocrinologychemistrybiology.proteinTumor necrosis factor alphaFemalemedicine.symptomInflammation MediatorsbusinessCorticosterone030217 neurology & neurosurgeryCell and Molecular Biologymedicine.drug
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The gelatinase MMP-9like is involved in regulation of LPS inflammatory response in Ciona robusta

2019

Matrix metalloproteinases (MMPs) are a family of endopeptidases collectively able to degrade the components of the extracellular matrix (ECM), with important roles in many biological processes, such as embryogenesis, normal tissue remodelling, angiogenesis and wound healing. New views on the function of MMPs reveal that they regulate inflammatory response and therefore might represent an early step in the evolution of the immune system. MMPs can affect the activity of cytokines involved in inflammation including TGF-β and TNF-α. MMPs are widely distributed in all kingdoms of life and have likely evolved from a single-domain protein which underwent successive rounds of duplications. In this …

0301 basic medicineLipopolysaccharidesModels MolecularAngiogenesisSettore BIO/05 - ZoologiaInflammationAquatic ScienceMatrix metalloproteinaseExtracellular matrixCiona robustaMatrix metalloproteinases (MMPs)MMP-2MMP-9PharynxInflammationLPS03 medical and health sciencesDownregulation and upregulationTransforming Growth Factor betamedicineEnvironmental ChemistryGelatinaseAnimalsCiona intestinalisPhylogenyInflammationbiologyTumor Necrosis Factor-alphafungi04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationMatrix MetalloproteinasesCell biologyCiona intestinalis030104 developmental biologyGelatinases040102 fisheries0401 agriculture forestry and fisheriesmedicine.symptomWound healing
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Determinants of fibrosis progression and regression in NASH

2017

Cirrhosis has become the major liver-related clinical endpoint in non-alcoholic steatohepatitis (NASH). However, progression to cirrhosis is less predictable in NASH than in other chronic liver diseases. This is due to the complex and multifactorial aetiology of NASH, which is determined by lifestyle and nutrition, multiple genetic and epigenetic factors, and a prominent role of hepatic and extrahepatic comorbidities. Thus, modest changes in these cofactors can also induce fibrosis regression, at least in patients with precirrhotic liver disease. Fibrogenesis in NASH correlates with, but is indirectly coupled to, classical inflammation, since fibrosis progression is driven by repetitive per…

0301 basic medicineLiver CirrhosisCirrhosisInflammationBioinformaticsCholangiocyte03 medical and health sciencesLiver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseClinical endpointMedicineHumansHepatologybusiness.industryDisease Managementmedicine.diseasePrognosis3. Good health030104 developmental biologyImmunologyHepatic stellate cellDisease Progression030211 gastroenterology & hepatologySteatohepatitismedicine.symptombusinessJournal of Hepatology
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Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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A randomized, placebo-controlled trial of cenicriviroc for treatment of nonalcoholic steatohepatitis with fibrosis

2018

The aim of this study was to evaluate cenicriviroc (CVC), a dual antagonist of C-C chemokine receptor types 2 and 5, for treatment of nonalcoholic steatohepatitis (NASH) with liver fibrosis. A randomized, double-blind, multinational phase 2b study enrolled subjects with NASH, a nonalcoholic fatty liver disease activity score [NAS] ≥4, and liver fibrosis (stages 1-3, NASH Clinical Research Network) at 81 clinical sites. Subjects (N = 289) were randomly assigned CVC 150 mg or placebo. Primary outcome was ≥2-point improvement in NAS and no worsening of fibrosis at year 1. Key secondary outcomes were: resolution of steatohepatitis and no worsening of fibrosis; improvement in fibrosis by ≥1 stag…

0301 basic medicineLiver CirrhosisMalePlacebo-controlled studyMedical Biochemistry and MetabolomicsGastroenterologyOral and gastrointestinallaw.inventionHepatitisNASH NAFLD CVC nonalcoholic fatty liver inflammationSteatohepatitis/Metabolic Liver Disease0302 clinical medicineRandomized controlled trialFibrosislawNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseeducation.field_of_studyCVCLiver DiseaseNASHImidazolesMiddle AgedTreatment OutcomeTolerabilityLiverSulfoxides6.1 PharmaceuticalsCCR5 Receptor Antagonists030211 gastroenterology & hepatologyOriginal ArticleFemalePatient SafetyAdultmedicine.medical_specialtyPopulationChronic Liver Disease and CirrhosisClinical Trials and Supportive ActivitiesClinical SciencesImmunologyPlacebo03 medical and health sciencesDouble-Blind MethodClinical ResearchInternal medicineNAFLDmedicinenonalcoholic fatty liverHumanseducationAgedHepatologyGastroenterology & Hepatologybusiness.industryEvaluation of treatments and therapeutic interventionsOriginal Articlesmedicine.diseaseequipment and suppliesSurgeryCVC; NAFLD; NASH; inflammation; nonalcoholic fatty liver030104 developmental biologyinflammationHuman medicineSteatohepatitisbusinessDigestive DiseasesBiomarkers
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